The objective of this study is to ivestigate the mechanisms by which behaviorally induced elevations blood pressure may interact with diet-induced hyperlipidemia to exacerbate the development of atherosclerosis in baboons (Papio cynocephalus anubis). To achieve this objective, we will use operant conditioning methods to include and maintain elevated blood pressures for 12 months in two groups of adult male baboons (minimum elevation of 25% over baseline); will induce hyperlipidemia in one of the two groups of conditioned baboons and also in a third group of adult male normotensive control baboons by feeding an atherogenic diet; and will assess and compare at autopsy the extent and type of atherosclerotic lesions in the cardiovascular systems of the hypertensive and normotensive animals. During the course of the study, we periodically will measure selected physiological, neuroendocrine, and metabolic responses in the three groups of baboons, including: (a) indices of cardivascular function (blood pressure, pulse pressure, heart rate); (b) neuroendocrine and humoral indicators of sympathetic nervous system arousal and stress (plasma catecholamines, cortisol, testosterone); (c) circulating mediators of blood pressure regulation (plasma renin activity, aldosterone, electrolytes); and (d) selected intervening variables implicated in the pathogeneisi of atherosclerosis (total serum cholesterol, LDL and HDL cholesterol). In conjunction with the morphometric and biochemical analysis of lesions, we will use correlation and regression procedures to estimate the association of elevated blood pressure with the extent of atherosclerosis. Finally, to seek possible underlying pathophysiological mechanisms relating behaviorally induced elevations in blood pressure and accelerated atherogenesis, we will assess the relationships between the physiological, humoral, and metabolic responses associated with behaviorally induced hypertension and the type and extent of atherosclerotic lesions. This study, a multidisciplinary effort involving scientists trained in experimental psychology, pathology, endocrinology, neuropharmacology, lipid biochemistry, and veterinary medicine, will provide new information concerning the role of chronic, environmentally induced hypertension in the etiology and pathogenesis of atherosclerosis.